Afferent and efferent components of the bronchial vagal branches in cats

Jammes, Yves; Fornaris, E.; Mei, N.; Barrat, E.

doi:10.1016/0165-1838(82)90037-6

Cited by 92 publications

(50 citation statements)

References 9 publications

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“…One of these factors is the activation of specific types of airway sensory nerves that are sensitive to an increase in temperature. The entire respiratory tract (from larynx to alveolar wall) is extensively innervated by vagal sensory nerves, of which the majority (z75%) are nonmyelinated (C-) afferent fibers (16). It is well documented that these bronchopulmonary C-fibers can be activated by various inhaled irritants and certain endogenous chemical mediators and play an important role in protecting the lung under normal and disease conditions (10)(11)(12).…”

Section: Discussionmentioning

confidence: 99%

Bronchoconstriction Triggered by Breathing Hot Humid Air in Patients with Asthma

Hayes¹,

Collins

Khosravi³

et al. 2012

Am J Respir Crit Care Med

131

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Rationale: Hyperventilation of hot humid air induces transient bronchoconstriction in patients with asthma; the underlying mechanism is not known. Recent studies showed that an increase in temperature activates vagal bronchopulmonary C-fiber sensory nerves, which upon activation can elicit reflex bronchoconstriction. Objectives: This study was designed to test the hypothesis that the bronchoconstriction induced by increasing airway temperature in patients with asthma is mediated through cholinergic reflex resulting from activation of these airway sensory nerves. Methods: Specific airway resistance (SR aw ) and pulmonary function were measured to determine the airway responses to isocapnic hyperventilation of humidified air at hot (49 8 C; HA) and room temperature (20-22 8 C; RA) for 4 minutes in six patients with mild asthma and six healthy subjects. A double-blind design was used to compare the effects between pretreatments with ipratropium bromide and placebo aerosols on the airway responses to HA challenge in these patients. Measurements and Main Results: SR aw increased by 112% immediately after hyperventilation of HA and by only 38% after RA in patients with asthma. Breathing HA, but not RA, triggered coughs in these patients. In contrast, hyperventilation of HA did not cause cough and increased SR aw by only 22% in healthy subjects; there was no difference between their SR aw responses to HA and RA challenges. More importantly, pretreatment with ipratropium completely prevented the HA-induced bronchoconstriction in patients with asthma. Conclusions: Bronchoconstriction induced by increasing airway temperature in patients with asthma is mediated through the cholinergic reflex pathway. The concomitant increase in cough response further indicates an involvement of airway sensory nerves, presumably the thermosensitive C-fiber afferents.Keywords: asthma; cough; bronchoconstriction; TRPV1; ipratropium It is extensively documented that breathing cold dry air induces bronchoconstriction in patients with asthma, which results primarily from injury of airway mucosa and release of various bronchoactive autacoids, such as leukotrienes and histamine (1). In contrast, the effects of an increase in temperature on the airway functions in patients with asthma is generally overlooked despite the fact that hyperthermia occurs frequently under normal and pathophysiological conditions. The most common causes of hyperthermia are elevated metabolic rate (e.g., during exercise) and hindered heat dissipation (e.g., in a warm environment). Hyperthermia can also occur under disease conditions, such as in patients suffering from severe fever. Furthermore, tissue inflammation is known to lead to local hyperemia and an increase in tissue temperature in the inflamed area (2, 3). A recent study has reported that the average end-expiratory temperature plateau (as an indirect measurement of the lung tissue temperature) is 2.7 8 C higher in children with asthma than that in healthy control subjects (4).An earlier study by Aitken and Marini ...

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Section: Discussionmentioning

confidence: 99%

Bronchoconstriction Triggered by Breathing Hot Humid Air in Patients with Asthma

Hayes¹,

Collins

Khosravi³

et al. 2012

Am J Respir Crit Care Med

131

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“…In healthy lungs, TRPV1 is selectively expressed in smalldiameter, slow-conducting nonmyelinated (C-) fibers that represent a majority (Ͼ75%) of vagal afferents innervating the lung and airways (30,31), and TRPA1 is found to be coexpressed with TRPV1 in a subset of these vagal C-fiber afferent nerves (5,40). Both TRPV1 and TRPA1 are recognized as the primary transducers located in the bronchopulmonary C-fiber sensory terminals that can be activated by a wide range of endogenous inflammatory mediators and activators (e.g., protons, hyperthermia, bradykinin, reactive oxygen radicals, etc.)…”

Section: Discussionmentioning

confidence: 99%

Calcium transient evoked by TRPV1 activators is enhanced by tumor necrosis factor-α in rat pulmonary sensory neurons

Gu²,

Lin³

et al. 2010

American Journal of Physiology-Lung Cellular and Molecular Phys

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Hu Y, Gu Q, Lin RL, Kryscio R, Lee LY. Calcium transient evoked by TRPV1 activators is enhanced by tumor necrosis factor-␣ in rat pulmonary sensory neurons. Am J Physiol Lung Cell Mol Physiol 299: L483-L492, 2010. First published July 16, 2010 doi:10.1152/ajplung.00111.2010.-TNF␣, a proinflammatory cytokine known to be involved in the pathogenesis of allergic asthma, has been shown to induce hyperalgesia in somatic tissue via a sensitizing effect on dorsal root ganglion neurons expressing transient receptor potential vanilloid type 1 receptor (TRPV1). Because TRPV1-expressing pulmonary sensory neurons play an important role in regulating airway function, this study was carried out to determine whether TNF␣ alters the sensitivity of these neurons to chemical activators. Responses of isolated nodose and jugular ganglion neurons innervating the rat lungs were determined by measuring the transient increase in intracellular Ca 2ϩ concentration ([Ca 2ϩ ]i). Our results showed the following. 1) A pretreatment with TNF␣ (50 ng/ml) for ϳ24 h increased significantly the peak ⌬[Ca 2ϩ ]i evoked by capsaicin (Cap) in these neurons. A pretreatment with the same concentration of TNF␣ for a longer duration (ϳ48 h) did not further increase the response, but pretreatment for a shorter duration (1 h) or with a lower concentration (25 ng/ml, 24 h) failed to enhance the Cap sensitivity.2) The same TNF␣ pretreatment also induced similar but less pronounced and less uniform increases in the responses to acid (pH 6.5-5.5), 2-aminoethoxydiphenyl borate (2-APB), a common activator of TRPV1, V2, and V3 channels, and allyl isothiocyanate (AITC), a selective activator of TRPA1 channel. 3) In sharp contrast, the responses to ATP, ACh, and KCl were not affected by TNF␣. 4) The TNF␣-induced hypersensitivity to Cap was not prevented by pretreatment with indomethacin (30 M). 5) The immunoreactivity to both TNF receptor types 1 and 2 were detected in rat vagal pulmonary sensory neurons. In conclusion, prolonged treatment with TNF␣ induces a pronounced potentiating effect on the responses of isolated pulmonary sensory neurons to TRPV1 activators. This action of TNF␣ may contribute in part to the airway hyperresponsiveness induced by this cytokine. intracellular calcium; pulmonary afferent; transient receptor potential vanilloid type 1; airway inflammation; asthma AN IMPORTANT ROLE OF TNF␣ in the pathogenesis of allergic asthma has been extensively documented (6,9,28,47). TNF␣ can be released from a variety of cell types in the airways, particularly macrophages, monocytes, and mast cells. TNF␣, either newly synthesized or preformed and stored constitutively within the mast cell granules, is coreleased with other potent mediators such as histamine and tryptase via the IgE-dependent mechanism (9, 21, 47). TNF␣ was detected in bronchoalveolar lavage fluid, sputum, exhaled breath condensate, and serum of asthmatic patients during asthmatic attack or following antigen inhalation challenge (12,33,39). Furthermore, it has been shown that TNF␣ is releas...

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“…We took advantage of the fact that motor nerves run exterior to the nodose ganglion as distinct superficial bundles at the ventral side (24,25); hence, afferent fibers were reached selectively in the center of the nodose ganglion by approaching the ganglion from the lateral side. Cats were killed after 1, 3, 5, or 28 days.…”

Section: Methodsmentioning

confidence: 99%

“…Therefore, we employed electron microscopy to study the relationships between nerve endings and smooth muscle cells and/or ICC. We also took advantage of the fact that motor nerves run exterior to the cat nodose ganglion as distinct superficial bundles at the ventral side (24,25); hence, afferent neurons can be reached selectively in the center of the nodose ganglion when approached from the lateral side.…”

mentioning

confidence: 99%

Survival dependency of intramuscular ICC on vagal afferent nerves in the cat esophagus

Huizinga¹,

Reed²,

Berezin³

et al. 2008

American Journal of Physiology-Regulatory, Integrative and Comp

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cells of Cajal (ICC) have been proposed as stretch receptors for vagal afferent nerves in the stomach based on immunohistochemical studies. The aim of the present study was to use electron microscopy and the anterograde degeneration technique to investigate ultrastructural features and survival dependency of ICC associated with vagal afferent innervation of the cat esophagus. This is the first report on the ultrastructural characteristics of ICC in the cat esophagus. Intramuscular ICC (ICC-IM) were identified throughout the musculature, whereas ICC in the myenteric plexus were rare. ICC-IM were particularly numerous in septa aligned with smooth muscle bundles. They were in synapse-like contact with nerve varicosities and in gap junction contact with smooth muscle cells. Smooth muscle cells also made contact with ICC through peg and socket junctions. Precision damage through small-volume injection of saline in the center of the nodose ganglion from the lateral side, known to selectively affect sensory nerves, was followed within 24 h by degeneration of a subset of nerve varicosities associated with ICC-IM, as well as degeneration of the associated ICC-IM. Smooth muscle cells were not affected. Nerves of Auerbachs plexus and associated ICC were not affected. In summary, ICC-IM aligning the esophageal muscle bundles form specialized synapse-like contacts with vagal afferent nerves as well as gap junction and peg-and-socket contacts with smooth muscle cells. This is consistent with a role of ICC-IM as stretch receptors associated with vagal afferent nerves; the ICC-vagal nerve interaction appears essential for the survival of the ICC. interstitial cells of Cajal; esophagus; stretch receptor; vagus; afferent innervation; intramuscular interstitial cells of Cajal FOR NORMAL ESOPHAGEAL function, the vagus nerves provide the major sensory and motor innervation to both striated and smooth muscle portions of the esophagus. Sensory pathways from the esophagus have been studied both electrophysiologically (40, 41) and by nerve tracing techniques (4,11,28). However, the precise location and structure of the sensory receptor(s) involved in control of esophageal motor function remain controversial. It is likely that more than one structurally and functionally distinct type of mechanoreceptor exists within the esophagus (4, 5, 8). As early as 1929, intraganglionic laminar nerve endings (IGLE) were considered candidates for esophageal stretch receptors (34). In an elegant study by Berthoud and Powley (4), intramuscular vagal afferents were shown to be positioned and structured as likely candidates for the gastric stretch receptor. Intramuscular arrays (IMA) enter circular or longitudinal muscle layers, run parallel to respective muscle fibers, and bifurcate to create an array of parallel terminal elements in stomach and sphincters (28). In the stomach, these terminal elements consist of interconnected parallel axonal telodendria that are arrayed in close proximity to one another and that form appositions with interstitial cells ...

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Afferent and efferent components of the bronchial vagal branches in cats

Cited by 92 publications

References 9 publications

Bronchoconstriction Triggered by Breathing Hot Humid Air in Patients with Asthma

Bronchoconstriction Triggered by Breathing Hot Humid Air in Patients with Asthma

Calcium transient evoked by TRPV1 activators is enhanced by tumor necrosis factor-α in rat pulmonary sensory neurons

Survival dependency of intramuscular ICC on vagal afferent nerves in the cat esophagus

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